Up-regulation of integrin beta3 expression in porcine vascular endothelial cells cultured in vitro by classical swine fever virus

Abstract

Classical swine fever (CSF) caused by virulent strains of classical swine fever virus (CSFV) is a haemorrhagic disease of pigs, characterized by disseminated intravascular coagulation, thrombocytopenia and immunosuppression. The cell adhesion molecule, integrin beta3, plays a central role in maintaining and regulating vascular permeability. In view of the haemorrhagic pathology of the disease, the effect of CSFV infection on integrin beta3 expression was investigated using the swine umbilical vein endothelial cell (SUVEC) line, in conjunction with quantitative PCR and Western blotting techniques. Following infection, the expression levels of integrin beta3 were significantly up-regulated along with corresponding transcription levels. The infected endothelial cells adhered onto immobilized extracellular matrix (ECM) with more extensive spreading than that of the control, and such interaction was strongly inhibited by an anti-integrin beta3 monoclonal antibody (mAb). This study revealed the up-regulation of integrin beta3 in vascular endothelial cells by CSFV infection, and cell adhesion molecules of this kind possibly play an important role in the changes of haemostatic balance in haemorrhagic pathology of CSF.